Poster Topical Area: Diet and Cancer

Location: Auditorium

Poster Board Number: 192

P07-006 - Consumption of black raspberries suppresses colitis and inflammation-associated colorectal cancer in mice

Monday, Jun 11
8:00 AM – 3:00 PM

Dietary strategies to reduce colonic inflammation and promote gut homeostasis may markedly reduce the risk of colitis-associated colorectal cancer (CAC). Black raspberries have demonstrated protective effects against colitis and/or colorectal cancer via their antioxidant and anti-inflammatory actions at the colon epithelium. Moreover, consumption of these foods can lead to changes in the composition of the gut microbiome. Objective: The goal of this study was to determine the impact of dietary supplementation with whole, freeze-dried raspberries on colitis and colon tumorigenesis in mice consuming a Western type diet.
Methods: C57BL/6J male mice were fed a standard diet (AIN93G), the total Western diet (TWD), TWD+5% (w/w) black raspberry powder (BRB) or TWD+10% (w/w) BRB for 16 weeks. All mice were dosed with axozymethane and provided 1% dextran sodium sulfate (DSS) in drinking water for 10 days to promote colonic inflammation and tumorigenesis.
Results: As expected, mice fed TWD alone had a markedly higher colitis disease activity index score as compared to mice provided the standard AIN93G diet. Also, consumption of the TWD markedly enhanced colon tumorigenesis compared to AIN93G controls. Supplementation of TWD with 10% BRB significantly reduced the symptoms of colitis compared to TWD alone. Moreover, by the period of recovery (14 days after DSS exposure), the disease activity index was significantly reduced in mice fed TWD supplemented with 5% or 10% BRB compared to TWD alone. Addition of 5% BRB significantly reduced tumor burden and 10% BRB reduced tumor multiplicity and burden, such that the cancer response was not different from the AIN93G-fed control mice.
Conclusion: Consumption of BRB at diet-relevant concentrations ameliorated symptoms of colitis promoted by consumption of TWD, most notably during the period of recovery from DSS-induced gut injury, and suppressed tumorigenesis in this mouse model of CAC.

Funding Source: USDA project # UTA-01178

CoAuthors: Sumira Phatak – Utah State University; Canyon Neal – Utah State University; Tess Armbrust – Utah State University; Daphne Rodriguez – Utah State University; Elizabeth Park – Utah State University; Michaela Brubaker – Utah State University; Kristina Krepinski – Utah State University; Melanie Athens – Utah State University; Korry Hintze – Utah State University

Abby Benninghoff

Associate Professor
Utah State University
Logan, Utah